Regulation of epithelial plasticity by miR-424 and miR-200 in a new prostate cancer metastasis model.
Regulation of epithelial plasticity by miR-424 and miR-200 in a new prostate cancer metastasis model.
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DOI：
10.1038/srep03151
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发表时间：
2013-11-06
影响因子：
4.6
通讯作者：
Zetter BR
中科院分区：
文献类型：
--
作者：
Banyard J;Chung I;Wilson AM;Vetter G;Le Béchec A;Bielenberg DR;Zetter BR
使用体内循环策略，我们从携带原位DU145人前列腺肿瘤的小鼠淋巴结（LN）中选择转移癌细胞。反复的转移选择（LN1-LN4）逐渐增加了上皮表型，导致肿瘤细胞间充质-上皮转化（MET）的新模式。DU145-LN4细胞间粘连增强，E-cadherin、EpCAM、细胞角蛋白18等多种上皮标志物表达升高，vimentin等间质标志物表达降低。DU145-LN4细胞中的MET伴随着miR-200家族的表达增加，miR-200c和miR-141的抗mir诱导EMT。MET也与miR-424的缺失相关。异位的短暂和稳定的miR-424表达诱导EMT，上皮标志物表达减少，细胞散射增加。我们的模型提供了体内自发MET的证据。我们发现这种细胞可塑性可以通过miR-424和miR-200家族的联合作用来介导。
Using an in vivo cycling strategy, we selected metastatic cancer cells from the lymph nodes (LN) of mice bearing orthotopic DU145 human prostate tumors. Repeated rounds of metastatic selection (LN1–LN4) progressively increased the epithelial phenotype, resulting in a new model of tumor cell mesenchymal-epithelial transition (MET). DU145-LN4 showed increased cell-cell adhesions, higher expression of multiple epithelial markers, such as E-cadherin, EpCAM and cytokeratin 18, and reduced expression of mesenchymal markers such as vimentin. The MET in DU145-LN4 cells was accompanied by increased expression of the miR-200 family, and antimiRs to miR-200c and miR-141 induced an EMT. MET also correlated with the loss of miR-424. Ectopic transient and stable miR-424 expression induced EMT, with reduced epithelial marker expression and increased cell scattering. Our model provides evidence for spontaneous MET in vivo. We show that this cellular plasticity can be mediated through the combined action of miR-424 and the miR-200 family.
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